title: A high-fat challenge increases airway inflammation and impairs bronchodilator recovery in asthma.
abstract: BACKGROUND
  Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown.
  
  
  OBJECTIVE
  To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma.
  
  
  METHODS
  Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-α, high-sensitivity C-reactive protein, and IL-6 concentrations.
  
  
  RESULTS
  In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV(1)/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV(1), % FVC, and FEV(1)/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal.
  
  
  CONCLUSIONS
  A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma.
authors.affiliation: Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, Australia. lisa.wood@newcastle.edu.au
authors.forename: Lisa G
authors.initials: LG
authors.lastname: Wood
authors.forename: Manohar L
authors.initials: ML
authors.lastname: Garg
authors.forename: Peter G
authors.initials: PG
authors.lastname: Gibson
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology* / Q000503:physiopathology*; D001980:Bronchi / Q000187:drug effects / Q000276:immunology / Q000503:physiopathology; D001993:Bronchodilator Agents / Q000494:pharmacology*; D004041:Dietary Fats / Q000008:administration & dosage* / Q000276:immunology / Q000494:pharmacology; D005227:Fatty Acids / Q000097:blood; D005260:Female; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects*; D007249:Inflammation / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology; D009765:Obesity / Q000150:complications / Q000276:immunology; D012137:Respiratory System / Q000187:drug effects* / Q000276:immunology / Q000503:physiopathology; D013183:Sputum / Q000276:immunology; D016896:Treatment Outcome
chemical_list: D001993:Bronchodilator Agents; D004041:Dietary Fats; D005227:Fatty Acids